Kim Hyun-Kyung, Choi Jun-Sub, Lee Seung Woo, Joo Choun-Ki, Joe Young Ae
Cancer Research Institute, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Department of Medical Lifescience, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
J Cell Biochem. 2017 May;118(5):1132-1143. doi: 10.1002/jcb.25732. Epub 2017 Jan 10.
The recombinant protein TK1-2, which consists of two kringle domains of tissue-type plasminogen activator (t-PA), inhibits angiogenesis and tumor growth. ɪn this study, we examined the anti-angiogenic activities of peptides derived from kringle 2 domain of t-PA to identify the functional core sequence. Seven peptides were constructed from the kringle 2 sequence, based on the structure and characteristics of amino acid residues, and were analyzed for their inhibitory effects on endothelial cells (ECs). Among them, TP-7 (derived from a β-sheet motif) potently inhibited proliferation, tube formation, and migration of ECs in a dose-dependent manner, whereas truncation of 3-9 amino acid residues from either N or C terminus of TP-7 abrogated its inhibitory effects on ECs. TP-7 also potently inhibited angiogenesis in a Matrigel plug assay in vivo. Moreover, TP-7 dose-dependently suppressed corneal neovascularization induced by an acute chemical burn in a rat model. At the molecular level, TP-7 inhibited VEGF- or bFGF-induced phosphorylation of FAK and ERK1/2 and drastically disrupted VEGF- or bFGF-induced formation of stress fibers and focal adhesion complexes. In addition, TP-7 markedly suppressed attachment and spreading of ECs on a collagen type I or fibronectin matrix. Adhesion of ECs to immobilized TP-7 increased dose-dependently, which was disrupted strongly by pretreatment with soluble TP-7 and slightly by an integrin α2β1-blocking antibody. These results suggest that TP-7 is a potent anti-angiogenic peptide in part affecting the integrin α2β1-dependent pathway and that it can be used for treatment of corneal neovascularization by targeting VEGF and non-VEGF pathways. J. Cell. Biochem. 118: 1132-1143, 2017. © 2016 Wiley Periodicals, Inc.
重组蛋白TK1-2由组织型纤溶酶原激活剂(t-PA)的两个kringle结构域组成,可抑制血管生成和肿瘤生长。在本研究中,我们检测了源自t-PA kringle 2结构域的肽的抗血管生成活性,以确定功能核心序列。根据氨基酸残基的结构和特征,从kringle 2序列构建了7种肽,并分析了它们对内皮细胞(ECs)的抑制作用。其中,TP-7(源自β-折叠基序)以剂量依赖的方式有效抑制ECs的增殖、管形成和迁移,而从TP-7的N端或C端截断3-9个氨基酸残基则消除了其对ECs的抑制作用。TP-7在体内基质胶栓试验中也有效抑制血管生成。此外,在大鼠模型中,TP-7以剂量依赖的方式抑制急性化学烧伤诱导的角膜新生血管形成。在分子水平上,TP-7抑制VEGF或bFGF诱导的FAK和ERK1/2磷酸化,并显著破坏VEGF或bFGF诱导的应力纤维和粘着斑复合物的形成。此外,TP-7显著抑制ECs在I型胶原或纤连蛋白基质上的附着和铺展。ECs与固定化TP-7的粘附呈剂量依赖性增加,可溶性TP-7预处理可强烈破坏这种粘附,而整合素α2β1阻断抗体则轻微破坏。这些结果表明,TP-7是一种有效的抗血管生成肽,部分影响整合素α2β1依赖性途径,并且它可通过靶向VEGF和非VEGF途径用于治疗角膜新生血管形成。《细胞生物化学杂志》118: 1132-1143, 2017。© 2016威利期刊公司